Zie ook onder alvleesklierkanker voor gerelateerde artikelen.
Raadpleeg ook literatuurlijst niet-toxische middelen en behandelingen specifiek bij alvleesklierkanker en galwegkanker van arts-bioloog drs. Engelbert Valstar.
19 augustus 2021: Zie ook dit artikel: https://kanker-actueel.nl/immuuntherapie-met-pertuzumab-plus-trastuzumab-herceptin-geeft-hoopvolle-resultaten-bij-patienten-met-gevorderde-uitgezaaide-galwegkanker-met-her2-mutatie-en-overexpressie.html
11 februari 2019: Bron: Precision Oncology
Alvleesklierkanker en galwegenkanker zijn een van de moeilijkst te behandelen vormen van kanker. Maar ook bij deze vormen van kanker blijkt een personalised aanpak op basis van DNA en RNA mutaties meer en meer de beste aanpak te kunnen zijn. (zie ook gerelateerde artikelen). Een onderzoeksteam van Nature Research maakte een overzichtsstudie over de ontwikkelingen binnen personalised medicine specifiek voor galwegenkanker en publiceerde dat eind vorig jaar in Precision Medicin.
Het studie rapport: Emerging role of precision medicine in biliary tract cancers is gratis in te zien en de onderzoekers bespreken een aantal veel voorkomende DNA en RNA mutaties en de daarop gerichte behandelingen waaronder immuuntherapie met anti-PD medicijnen. Hier een grafiek uit die studie van hoeveel mutaties er wel niet zijn.
References belonging to emerging role of precision medicine in biliary tract cancers
References
- 1.
Razumilava, N. & Gores, G. J. Building a staircase to precision medicine for biliary tract cancer. Nat. Genet. 47, 967 (2015).
- 2.
Valle, J. et al. Cisplatin plus gemcitabine versus gemcitabine for biliary tract cancer. N. Engl. J. Med. 362, 1273–1281 (2010).
- 3.
Hendriks, Y. M. et al. Diagnostic approach and management of Lynch syndrome (hereditary nonpolyposis colorectal carcinoma): a guide for clinicians. Cancer J. Clin. 56, 213–225 (2006).
- 4.
Cortes-Ciriano, I., Lee, S., Park, W. Y., Kim, T. M. & Park, P. J. A molecular portrait of microsatellite instability across multiple cancers. Nat. Commun. 8, 15180 (2017).
- 5.
Herman, J. G. et al. Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma. Proc. Natl Acad. Sci. USA 95, 6870–6875 (1998).
- 6.
Ligtenberg, M. J. et al. Heritable somatic methylation and inactivation of MSH2 in families with Lynch syndrome due to deletion of the 3′ exons of TACSTD1. Nat. Genet. 41, 112–117 (2009).
- 7.
Chalmers, Z. R. et al. Analysis of tumor mutation burden (TMB) in >51,000 clinical cancer patients to identify novel non-coding PMS2 promoter mutations associated with increased TMB. J. Clin. Oncol. 34, 9572–9572 (2016).
- 8.
Volinia, S. et al. A microRNA expression signature of human solid tumors defines cancer gene targets. Proc. Natl Acad. Sci. USA 103, 2257–2261 (2006).
- 9.
Lemery, S., Keegan, P. & Pazdur, R. First FDA approval agnostic of cancer site—when a biomarker defines the indication. N. Engl. J. Med 377, 1409–1412 (2017).
- 10.
Silva, V. W. et al. Biliary carcinomas: pathology and the role of DNA mismatch repair deficiency. Chin. Clin. Oncol. 5, 62 (2016).
- 11.
Buecher, B. et al. Role of microsatellite instability in the management of colorectal cancers. Dig. Liver Dis. 45, 441–449 (2013).
- 12.
Umar, A. et al. Revised Bethesda Guidelines for hereditary nonpolyposis colorectal cancer (Lynch syndrome) and microsatellite instability. J. Natl Cancer Inst. 96, 261–268 (2004).
- 13.
Schumacher, T. N. & Schreiber, R. D. Neoantigens in cancer immunotherapy. Science 348, 69–74 (2015).
- 14.
Goodman, A. M. et al. Tumor mutational burden as an independent predictor of response to immunotherapy in diverse cancers. Mol. Cancer Ther. 16, 2598–2608 (2017).
- 15.
Nakamura, H. et al. Genomic spectra of biliary tract cancer. Nat. Genet. 47, 1003–1010 (2015).
- 16.
Sabbatino, F. et al. PD-L1 and HLA Class I antigen expression and clinical course of the disease in intrahepatic cholangiocarcinoma. Clin. Cancer Res. 22, 470–478 (2016).
- 17.
Fontugne, J. et al. PD-L1 expression in perihilar and intrahepatic cholangiocarcinoma. Oncotarget 8, 24644–24651 (2017).
- 18.
Bang, Y. J. et al. 525 Safety and efficacy of pembrolizumab (MK-3475) in patients (pts) with advanced biliary tract cancer: interim results of KEYNOTE-028. Eur. J. Cancer 51, S112.
- 19.
Barrett, M. T. et al. Genomic amplification of 9p24.1 targeting JAK2, PD-L1, and PD-L2 is enriched in high-risk triple negative breast cancer. Oncotarget 6, 26483–26493 (2015).
- 20.
Cancer Genome Atlas Research, N. Comprehensive molecular characterization of gastric adenocarcinoma. Nature 513, 202–209 (2014).
- 21.
Green, M. R. et al. Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma. Blood 116, 3268–3277 (2010).
- 22.
Wang, L. et al. Programmed death-ligand 1 is upregulated in intrahepatic lymphoepithelioma-like cholangiocarcinoma. Oncotarget 7, 69749–69759 (2016).
- 23.
Arai, Y. et al. Fibroblast growth factor receptor 2 tyrosine kinase fusions define a unique molecular subtype of cholangiocarcinoma. Hepatology 59, 1427–1434 (2014).
- 24.
Graham, R. P. et al. Fibroblast growth factor receptor 2 translocations in intrahepatic cholangiocarcinoma. Hum. Pathol. 45, 1630–1638 (2014).
- 25.
Javle, M. et al. Biliary cancer: utility of next-generation sequencing for clinical management. Cancer 122, 3838–3847 (2016).
- 26.
Farshidfar, F. et al. Integrative genomic analysis of cholangiocarcinoma identifies distinct IDH-mutant molecular profiles. Cell Rep. 19, 2878–2880 (2017).
- 27.
Guagnano, V. et al. Discovery of 3-(2,6-dichloro-3,5-dimethoxy-phenyl)-1-{6-[4-(4-ethyl-piperazin-1-yl)-phenylamin o]-pyrimidin-4-yl}-1-methyl-urea (NVP-BGJ398), a potent and selective inhibitor of the fibroblast growth factor receptor family of receptor tyrosine kinase. J. Med. Chem. 54, 7066–7083 (2011).
- 28.
Javle, M. et al. Phase II Study of BGJ398 in patients with FGFR-altered advanced cholangiocarcinoma. (2017). J Clin Oncol. 10.1200/JCO.2017.75.5009.
- 29.
Gilbert, J. A. BGJ398 for FGFR-altered advanced cholangiocarcinoma. Lancet Oncol. 10.1016/S1470-2045(17)30902-6 (2017).
- 30.
Perwad, F., Zhang, M. Y., Tenenhouse, H. S. & Portale, A. A. Fibroblast growth factor 23 impairs phosphorus and vitamin D metabolism in vivo and suppresses 25-hydroxyvitamin D-1alpha-hydroxylase expression in vitro. Am. J. Physiol. Ren. Physiol. 293, F1577–F1583 (2007).
- 31.
Gattineni, J. et al. FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am. J. Physiol. Ren. Physiol. 297, F282–F291 (2009).
- 32.
Saleh, M. et al. Abstract CT111: preliminary results from a phase 1/2 study of INCB054828, a highly selective fibroblast growth factor receptor (FGFR) inhibitor, in patients with advanced malignancies. Cancer Res. 77, CT111–CT111 (2017).
- 33.
Hall, T. G. et al. Preclinical activity of ARQ 087, a novel inhibitor targeting FGFR dysregulation. PLoS One 11, e0162594 (2016).
- 34.
Papadopoulos, K. P. et al. A Phase 1 study of ARQ 087, an oral pan-FGFR inhibitor in patients with advanced solid tumours. Br. J. Cancer 117, 1592–1599 (2017).
- 35.
Mazzaferro, V. et al. ARQ 087, an oral pan-fibroblast growth factor receptor (FGFR) inhibitor, in patients (pts) with advanced intrahepatic cholangiocarcinoma (iCCA) with FGFR2 genetic aberrations. J. Clin. Oncol. 35, 4017–4017 (2017).
- 36.
Goyal, L. et al. Polyclonal secondary FGFR2 mutations drive acquired resistance to FGFR inhibition in patients with FGFR2 fusion-positive cholangiocarcinoma. Cancer Discov. 7, 252–263 (2017).
- 37.
Kim, S. T. et al. Prospective blinded study of somatic mutation detection in cell-free DNA utilizing a targeted 54-gene next generation sequencing panel in metastatic solid tumor patients. Oncotarget 6, 40360–40369 (2015).
- 38.
Song, K. H., Li, T., Owsley, E., Strom, S. & Chiang, J. Y. Bile acids activate fibroblast growth factor 19 signaling in human hepatocytes to inhibit cholesterol 7alpha-hydroxylase gene expression. Hepatology 49, 297–305 (2009).
- 39.
Holt, J. A. et al. Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis. Genes Dev. 17, 1581–1591 (2003).
- 40.
Arnold, A. et al. Genome wide DNA copy number analysis in cholangiocarcinoma using high resolution molecular inversion probe single nucleotide polymorphism assay. Exp. Mol. Pathol. 99, 344–353 (2015).
- 41.
Kaibori, M. et al. Increased FGF19 copy number is frequently detected in hepatocellular carcinoma with a complete response after sorafenib treatment. Oncotarget 7, 49091–49098 (2016).
- 42.
Bengala, C. et al. Sorafenib in patients with advanced biliary tract carcinoma: a phase II trial. Br. J. Cancer 102, 68–72 (2010).
- 43.
Luo, X. et al. Effectiveness and safety of sorafenib in the treatment of unresectable and advanced intrahepatic cholangiocarcinoma: a pilot study. Oncotarget 8, 17246–17257 (2017).
- 44.
Chakunta, H. R., Sunderkrishnan, R., Kaplan, M. A. & Mostofi, R. Cholangiocarcinoma: treatment with sorafenib extended life expectancy to greater than four years. J. Gastrointest. Oncol. 4, E30–E32 (2013).
- 45.
Tsukada, Y. et al. Histone demethylation by a family of JmjC domain-containing proteins. Nature 439, 811–816 (2006).
- 46.
Xu, W. et al. Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenases. Cancer Cell 19, 17–30 (2011).
- 47.
Borger, D. R. et al. Frequent mutation of isocitrate dehydrogenase (IDH)1 and IDH2 in cholangiocarcinoma identified through broad-based tumor genotyping. Oncologist 17, 72–79 (2012).
- 48.
Jiao, Y. et al. Exome sequencing identifies frequent inactivating mutations in BAP1, ARID1A and PBRM1 in intrahepatic cholangiocarcinomas. Nat. Genet. 45, 1470–1473 (2013).
- 49.
Wang, P. et al. Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas. Oncogene 32, 3091–3100 (2013).
- 50.
Zhu, A. X. et al. Genomic profiling of intrahepatic cholangiocarcinoma: refining prognosis and identifying therapeutic targets. Ann. Surg. Oncol. 21, 3827–3834 (2014).
- 51.
Yoshikawa, D. et al. Clinicopathological and prognostic significance of EGFR, VEGF, and HER2 expression in cholangiocarcinoma. Br. J. Cancer 98, 418–425 (2008).
- 52.
Yang, X. et al. Characterization of EGFR family gene aberrations in cholangiocarcinoma. Oncol. Rep. 32, 700–708 (2014).
- 53.
Javle, M. et al. HER2/neu-directed therapy for biliary tract cancer. J. Hematol. Oncol. 8, 58 (2015).
- 54.
Lee, J. et al. Gemcitabine and oxaliplatin with or without erlotinib in advanced biliary-tract cancer: a multicentre, open-label, randomised, phase 3 study. Lancet Oncol. 13, 181–188 (2012).
- 55.
Borad, M. J. et al. Integrated genomic characterization reveals novel, therapeutically relevant drug targets in FGFR and EGFR pathways in sporadic intrahepatic cholangiocarcinoma. PLoS Genet. 10, e1004135 (2014).
- 56.
Li, M. et al. Whole-exome and targeted gene sequencing of gallbladder carcinoma identifies recurrent mutations in the ErbB pathway. Nat. Genet. 46, 872–876 (2014).
- 57.
Deshpande, V. et al. Mutational profiling reveals PIK3CA mutations in gallbladder carcinoma. BMC Cancer 11, 60 (2011).
- 58.
Churi, C. R. et al. Mutation profiling in cholangiocarcinoma: prognostic and therapeutic implications. PLoS One 9, e115383 (2014).
- 59.
Bekaii-Saab, T. et al. Multi-institutional phase II study of selumetinib in patients with metastatic biliary cancers. J. Clin. Oncol. 29, 2357–2363 (2011).
- 60.
Brea, E. J. et al. Kinase regulation of human MHC class I molecule expression on cancer cells. Cancer Immunol. Res. 4, 936–947 (2016).
- 61.
Sullivan, R. J. et al. Atezolizumab (A) + cobimetinib (C) + vemurafenib (V) in BRAFV600-mutant metastatic melanoma (mel): updated safety and clinical activity. J. Clin. Oncol. 35, 3063–3063 (2017).
- 62.
Ewald, F. et al. Dual Inhibition of PI3K-AKT-mTOR- and RAF-MEK-ERK-signaling is synergistic in cholangiocarcinoma and reverses acquired resistance to MEK-inhibitors. Invest. New Drugs 32, 1144–1154 (2014).
- 63.
Miyamoto, M. et al. Prognostic significance of overexpression of c-Met oncoprotein in cholangiocarcinoma. Br. J. Cancer 105, 131–138 (2011).
- 64.
Yakes, F. M. et al. Cabozantinib (XL184), a novel MET and VEGFR2 inhibitor, simultaneously suppresses metastasis, angiogenesis, and tumor growth. Mol. Cancer Ther. 10, 2298–2308 (2011).
- 65.
Goyal, L. et al. A phase 2 and biomarker study of cabozantinib in patients with advanced cholangiocarcinoma. Cancer 123, 1979–1988 (2017).
- 66.
Riener, M. O., Bawohl, M., Clavien, P. A. & Jochum, W. Rare PIK3CA hotspot mutations in carcinomas of the biliary tract. Genes Chromosomes Cancer 47, 363–367 (2008).
- 67.
Shigematsu, H., Takahashi, T., Minna, J. D., Gazdar, A. F. & Wistuba, I. I. PIK3CA mutations in gallbladder cancers. Cancer Res. 66, 50–51 (2006).
- 68.
Yeung, Y. et al. K-Ras mutation and amplification status is predictive of resistance and high basal pAKT is predictive of sensitivity to everolimus in biliary tract cancer cell lines. Mol. Oncol. 11, 1130–1142 (2017).
- 69.
Jin, L. et al. Anti-tumor effects of NVP-BKM120 alone or in combination with MEK162 in biliary tract cancer. Cancer Lett. 411, 162–170 (2017).
- 70.
Ahn, D. H. et al. Results of an abbreviated phase-II study with the Akt inhibitor MK-2206 in patients with advanced biliary cancer. Sci. Rep. 5, 12122 (2015).
- 71.
Zhang, Y. et al. A novel PI3K/AKT signaling axis mediates Nectin-4-induced gallbladder cancer cell proliferation, metastasis and tumor growth. Cancer Lett. 375, 179–189 (2016).
- 72.
Challita-Eid, P. M. et al. Enfortumab vedotin antibody-drug conjugate targeting nectin-4 is a highly potent therapeutic agent in multiple preclinical cancer models. Cancer Res. 76, 3003–3013 (2016).
- 73.
Ross, J. S. et al. New routes to targeted therapy of intrahepatic cholangiocarcinomas revealed by next-generation sequencing. Oncologist 19, 235–242 (2014).
- 74.
Tadokoro, H., Shigihara, T., Ikeda, T., Takase, M. & Suyama, M. Two distinct pathways of p16 gene inactivation in gallbladder cancer. World J. Gastroenterol. 13, 6396–6403 (2007).
- 75.
Kagohara, L. T. et al. Global and gene-specific DNA methylation pattern discriminates cholecystitis from gallbladder cancer patients in Chile. Future Oncol. 11, 233–249 (2015).
- 76.
Ahn, D. H. et al. Next-generation sequencing survey of biliary tract cancer reveals the association between tumor somatic variants and chemotherapy resistance. Cancer 122, 3657–3666 (2016).
- 77.
Simbolo, M. et al. Multigene mutational profiling of cholangiocarcinomas identifies actionable molecular subgroups. Oncotarget 5, 2839–2852 (2014).
- 78.
Golan, T. et al. Overall survival and clinical characteristics of BRCA-associated cholangiocarcinoma: A Multicenter Retrospective Study. Oncologist 22, 804–810 (2017).
- 79.
Xie, Y. et al. Response of BRCA1-mutated gallbladder cancer to olaparib: a case report. World J. Gastroenterol. 22, 10254–10259 (2016).
- 80.
Shen, J. et al. ARID1A deficiency impairs the DNA damage checkpoint and sensitizes cells to PARP inhibitors. Cancer Discov. 5, 752–767 (2015).
- 81.
Robertson, A. G. et al. Integrative analysis identifies four molecular and clinical subsets in uveal melanoma. Cancer Cell 32, 204–220 (2017).
- 82.
Dalmasso, C. et al. Patterns of chromosomal copy-number alterations in intrahepatic cholangiocarcinoma. BMC Cancer 15, 126 (2015).
- 83.
Yang, B., House, M. G., Guo, M., Herman, J. G. & Clark, D. P. Promoter methylation profiles of tumor suppressor genes in intrahepatic and extrahepatic cholangiocarcinoma. Mod. Pathol. 18, 412 (2004).
- 84.
Jusakul, A. et al. Whole-genome and epigenomic landscapes of etiologically distinct subtypes of cholangiocarcinoma. Cancer Discov. 7, 1116–1135 (2017).
- 85.
Delmore, J. E. et al. BET bromodomain inhibition as a therapeutic strategy to target c-Myc. Cell 146, 904–917 (2011).
- 86.
Zhu, H. et al. BET bromodomain inhibition promotes antitumor immunity by suppressing PD-L1 expression. Cell Rep. 16, 2829–2837 (2016).
- 87.
Okaro, A. C., Deery, A. R., Hutchins, R. R. & Davidson, B. R. The expression of antiapoptotic proteins Bcl-2, Bcl-X(L), and Mcl-1 in benign, dysplastic, and malignant biliary epithelium. J. Clin. Pathol. 54, 927–932 (2001).
- 88.
Isomoto, H. et al. Sustained IL-6/STAT-3 signaling in cholangiocarcinoma cells due to SOCS-3 epigenetic silencing. Gastroenterology 132, 384–396 (2007).
- 89.
Yoon, J. H. et al. Bile acids inhibit Mcl-1 protein turnover via an epidermal growth factor receptor/Raf-1-dependent mechanism. Cancer Res. 62, 6500–6505 (2002).
- 90.
Wang, W. et al. FXR agonists enhance the sensitivity of biliary tract cancer cells to cisplatin via SHP dependent inhibition of Bcl-xL expression. Oncotarget 7, 34617–34629 (2016).
- 91.
Tannapfel, A. et al. Frequency ofp16(INK4A) alterations and K-ras mutations in intrahepatic cholangiocarcinoma of the liver. Gut 47, 721–727 (2000).
- 92.
Imamura, F. et al. Monitoring of treatment responses and clonal evolution of tumor cells by circulating tumor DNA of heterogeneous mutant EGFR genes in lung cancer. Lung Cancer 94, 68–73 (2016).
- 93.
Zill, O. A. et al. Cell-Free DNA next-generation sequencing in pancreatobiliary carcinomas. Cancer Discov. 5, 1040–1048 (2015).
- 94.
Sato, T. et al. Long-term expansion of epithelial organoids from human colon, adenoma, adenocarcinoma, and Barrett’s epithelium. Gastroenterology 141, 1762–1772 (2011).
- 95.
Shalem, O. et al. Genome-scale CRISPR-Cas9 knockout screening in human cells. Science 343, 84–87 (2014).
- 96.
Primrose, J. N. et al. Adjuvant capecitabine for biliary tract cancer: the BILCAP randomized study. J. Clin. Oncol. 35, 4006–4006 (2017).
- 97.
Gu, T. L. et al. Survey of tyrosine kinase signaling reveals ROS kinase fusions in human cholangiocarcinoma. PLoS One 6, e15640 (2011).
- 98.
Lee, K. H. et al. Clinical and pathological significance of ROS1 expression in intrahepatic cholangiocarcinoma. BMC Cancer 15, 721 (2015).
- 99.
Hyman, D. M. et al. The efficacy of larotrectinib (LOXO-101), a selective tropomyosin receptor kinase (TRK) inhibitor, in adult and pediatric TRK fusion cancers. J. Clin. Oncol. 35, LBA2501–LBA2501 (2017).
- 100.
Drilon, A. et al. Safety and antitumor activity of the multitargeted Pan-TRK, ROS1, and ALK inhibitor entrectinib: combined results from two phase ITrials (ALKA-372-001 and STARTRK-1). Cancer Discov. 7, 400–409 (2017).
Author information
Affiliations
-
Division of Hematology/Oncology, Department of Medicine, Mayo Clinic, Scottsdale, AZ, USA
- James M. Bogenberger
- , Thomas T. DeLeon
- , Mansi Arora
- , Daniel H. Ahn
- & Mitesh J. Borad
-
Department of Molecular Medicine, Mayo Clinic, Rochester, MN, USA
- Mitesh J. Borad
-
Mayo Clinic Cancer Center, Mayo Clinic, Phoenix, AZ, USA
- Mitesh J. Borad
Authors
-
Search for James M. Bogenberger in:
-
Search for Thomas T. DeLeon in:
-
Search for Mansi Arora in:
-
Search for Daniel H. Ahn in:
-
Search for Mitesh J. Borad in:
Contributions
All authors made contributions in preparing this review article, and read/approved the final manuscript.
Competing interests
J.M.B. owns purchased stock of Array BioPharma, Arqule Inc., Clovis Oncology, Intercept Pharmaceuticals, and Seattle Genetics. M.J.B. owns purchased stock of Intercept Pharmaceuticals. The remaining authors declare no competing interests.
Corresponding author
Correspondence to Mitesh J. Borad.
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Gerelateerde artikelen
- ASCO 2024: abstracten van ASCO 2024 gerelateerd aan alvleesklierkanker en galwegenkanker
- Chemo (oxaliplatin plus gemcitabine) na operatie bij galwegkanker geeft 25 maanden extra overall overleving (50 vs 75 maanden ) maar wordt afgedaan als zou chemo zinloos zijn copy 1
- Durvalumab gegeven naast gemcitabine plus cisplatine geeft betere overall overleving voor nieuw gediagnosticeerde gevorderde galwegkanker
- Galwegstents via de buikwand en HAIP - intra-arteriële chemotherapie voorkomen minder complicaties en verlengen overall overleving bij patienten met gevorderde en inoperabele galwegenkanker
- Immuuntherapie met pertuzumab plus trastuzumab (herceptin) geeft hoopvolle resultaten bij patiënten met gevorderde uitgezaaide galwegkanker met HER2-mutatie en overexpressie
- ivosidenib, een medicijn gericht op de IDH1 mutatie geeft hoopvolle resultaten bij zwaar voorbehandelde patienten met uitgezaaide galwegenkanker
- Panitumumab in combinatie met cisplatin en gemcitabine geeft beduidend minder overall overleving (13 vs 20 maanden) bij galwegkanker met KRAS wild-type
- PDT - Photo Dynamische Therapie als palliatieve behandeling van inoperabele galwegenkanker verlengt hoog significant mediane overleving bij inoperabele uitgezaaide galwegkanker blijkt uit gerandomiseerde studies. Artikel update 6 februari 2010
- Pemigatinib, een FGFR remmer, voor patiënten met eerder behandelde galwegenkanker geeft bij patienten met een FGFR2-mutatie uitstekende resultaten met een objectieve respons van 35 procent.versus 0 procent bij wie geen FGFR2 mutatie had
- Personalised medicine op basis van DNA en RNA mutaties voor bv. immuuntherapie met anti-PD en gerichte behandelingen lijkt voor galwegenkanker zeker zinvol aldus overzichtsstudie
- Specifieke bloedwaarden en biomarkers die wijzen op veroudering van immuunsysteem (immunosenescentie-biomarkers) plus basale EGF-concentratie in bloed resulteerden in goede voorspellers van het succes van het CIMAvax-EGF vaccin bij gevorderde longkanker c
- TACE - Trans Arteriele Chemo Embolisatie met gemcitabine plus cisplatin geeft bij uitgezaaide galwegkanker significant langere levensduur dan TACE met alleen gemcitabine. d.d. 6 februari 2010
- TAS-120 geeft uitstekende resultaten bij verschillende studies met solide tumoren waaronder galwegkanker
- TAS-120 - futibatinib geeft veelbelovende resultaten bij patienten met in lever uitgezaaide galwegenkanker met fibroblast growth factor receptor 2 (FGFR2) en T53 mutaties copy 1
Plaats een reactie ...
Reageer op "Personalised medicine op basis van DNA en RNA mutaties voor bv. immuuntherapie met anti-PD en gerichte behandelingen lijkt voor galwegenkanker zeker zinvol aldus overzichtsstudie"